Correspondence

Lundblad, Lennart K. A.; Thompson-Figueroa, John; Leclair, Timothy; Sullivan, Michael J.; Poynter, Matthew E.; Irvin, Charles G.; Bates, Jason H. T.

doi:10.1164/ajrccm.172.12.1605b

Cited by 3 publications

(4 citation statements)

References 7 publications

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“…The copyright holder for this preprint this version posted October 21, 2022. ; https://doi.org/10.1101/2022.10.21.513138 doi: bioRxiv preprint proinflammatory and prooxidative actions (62), and its overexpression has been associated with emphysema (63). TNF-α can directly contribute to cytolysis, together with the cytotoxic granzyme B (64) and in synergy with IFN-γ (65).…”

Section: Discussionmentioning

confidence: 99%

“…Greater production of TNF-α, IFN-γ and granzyme B by CD8 + T cells triggered by the interaction with fibrocytes is consistent with previous studies showing enhanced production of Tc1 cytokines and cytotoxic molecules by CD8 + T cells purified from patients with COPD (13,60,61), suggesting that local interactions with cells such as fibrocytes may play a pivotal role in CD8 polarization in COPD. In particular, TNF-α has proinflammatory and prooxidative actions (62), and its overexpression has been associated with emphysema (63). TNF-α can directly contribute to cytolysis, together with the cytotoxic granzyme B (64) and in synergy with IFN-γ (65).…”

Section: Discussionmentioning

confidence: 99%

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Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response

Eyraud

Maurat

Sac-Epee

et al. 2022

Preprint

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The peri-bronchial zone of chronic obstructive pulmonary disease (COPD) is the site of extensive infiltration of immune cell, allowing persistent contacts between resident cells and immune cells. Tissue fibrocytes interaction with CD8+T cells and its consequences were investigated. We show that interactions beween both cell types are more frequent in distal airways from COPD patients compared to those of control subjects. Tissular CD8+T cells from COPD patients promote fibrocyte chemotaxis via the CXCL8-CXCR1/2 axis. CD8+T cells establish short-term interactions with fibrocytes, that trigger CD8+T cell proliferation in a CD54- and CD86-dependent manner, as well as pro-inflammatory cytokines production. A computational model accurately predicts histologicalex vivocharacteristics and allows to monitors disease evolution. Overall, our study reveals that local interactions between fibrocytes and CD8+T cells may comromise the balance between protective immunity and chronic inflammation in bronchi of COPD patients.TeaserFibrocytes/CD8+T cells interactions cause inflammation through a maintained pathophysiological loop in bronchi of COPD patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response

Eyraud

Maurat

Sac-Epee

et al. 2022

Preprint

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“…На даний час ФНП-α визнають центральним медіатором серед ши-ро кого спектра фізіологічних та імуно логічних функцій. Ця молекула проявляє різні біологічні ефекти, в тому числі індукує цитотоксичні ефекти на ендотеліальні кліти ни, підсилює до них адгезію нейтрофілів шляхом підвищення вироблення хемокінів та адгезивних молекул, збільшує судинну проникність через активацію нейтрофілів, а також стимулює продукування інших прозапальних цитокінів (інтерлейкінів 1, 6, 8) [2,3].…”

Section: вступunclassified

Pathogenetic Mechanisms of Lung Injury

Marushchak¹,

Krynytska²,

Gabor³

et al. 2016

IJMMR

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Тернопільський державний медичний універсиТеТ імені і. Я. ГорбачевськоГо Вступ. на сучасному етапі розвитку медико-біологічної науки увага більшості дослідників прикута до ключових механізмів багатьох захворювань людини, які тісно пов'язані з порушенням клітинної смерті. однією з провідних причин дисрегуляції танатогенної програми клітин є активація біологічних ефектів фактора некрозу пухлин альфа. Мета. узагальнити існуючі наукові дані щодо внеску метаболітів кисню і монооксиду нітрогену в механізми легеневого ураження. Методи. аналіз літературних даних щодо механізму легеневого ураження. Результати й висновки. у зв'язку з вищесказаним, актуальною є проблема розуміння сигналів та механізмів, відповідальних за регулювання процесів вільнорадикального окиснення і системи антиоксидантного захисту, роль про-та протизапальних молекул, вплив активних метаболітів на процеси репарації і виживання клітин респіраторного тракту при гострих ураженнях легень. розуміння суті даних процесів дозволить поглибити існуючі й отримати нові знання при легеневій патології.

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“…It is well documented that TNF is a crucial proinflammatory cytokine having a predominant role in COPD pathogenesis [132,133], leading to up-or downregulation of various genes [134,135].…”

Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 99%

Genetics of Chronic Obstructive Pulmonary Disease, Beyond a1-Antitrypsin Deficiency

Sampsonas

Karkoulias²,

Kaparianos³

et al. 2006

CMC

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It is known that only 10-20% of smokers develop COPD, implying that apart from environmental features, additional factors such as genetic variability contribute to smoke susceptibility. This proposal is in compatibility with the "Dutch Hypothesis", formulated in the early 60's. Alpha-1-antitrypsin gene was implicated in the pathogenesis of COPD, especially the homozygous state of z allele. Since then many other genes have stepped forward as possible contributors to COPD development. In the present review we attempt to summarize the majority of these, including the genes of matrix metalloproteinases and their inhibitors, elastin, serpine2, tumor necrosis factor - a, transforming growth factor beta, a variety of interleukins and their receptors and antagonists, high affinity IgE receptor , human calcium-activated chloride channel 1, heme oxygenase, vascular endothelial growth factor, microsomal epoxide hydrolase, glutathione S-transferase, cytochrome P45O, superoxide dismutase, vitamin D binding protein, beta2-adrenergic receptor, Toll like receptor, human B defensins, mucins, cystic fibrosis transmembrane regulator, surfactant protein and Nuclear Factor E2 Related Factor 2.

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Correspondence

Cited by 3 publications

References 7 publications

Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response

Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response

Pathogenetic Mechanisms of Lung Injury

Genetics of Chronic Obstructive Pulmonary Disease, Beyond a1-Antitrypsin Deficiency

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Correspondence

Cited by 3 publications

References 7 publications

Short-range interactions between fibrocytes and CD8+T cells in COPD bronchial inflammatory response

Short-range interactions between fibrocytes and CD8+T cells in COPD bronchial inflammatory response

Pathogenetic Mechanisms of Lung Injury

Genetics of Chronic Obstructive Pulmonary Disease, Beyond a1-Antitrypsin Deficiency

Contact Info

Product

Resources

About

Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response

Short-range interactions between fibrocytes and CD8⁺T cells in COPD bronchial inflammatory response